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Coccidioidomycosis is a common fungal infection in people living with HIV-1, particularly in southwest regions of the United States where the Coccidioides sp. is endemic, but rates of infection have significantly declined in the era of potent combination antiretroviral therapy (cART). Natural coccidioidomycosis also occurs in outdoor-housed macaques residing in the southwestern states that are utilized in biomedical research. Here, we report on a recrudescent case of previously treated, naturally occurring coccidioidomycosis in a pigtail macaque that was experimentally infected with simian immunodeficiency virus (SIV) and virally suppressed on cART. Coccidioides IgG antibody titer became detectable before discontinuation of cART, but symptomatic coccidioidomycosis developed subsequent to cART withdrawal. This animal was screened and treated in accordance with the guidelines for the prevention and treatment of coccidioidomycosis, suggesting that macaques with a history of coccidioidomycosis should be excluded from enrollment in HIV studies. Continual monitoring for known endemic pathogens based on the colony of origin is also recommended for animals utilized for HIV/AIDS research. [ABSTRACT FROM AUTHOR]

Fifteen pigtail macaques were enrolled in a hepatitis B virus (HBV) vaccine study and infected with SIV as a model to determine if HIV infection may impact immunogenicity of this vaccine (Supplementary Table S1). Our earlier and follow-up results reported here show that prior coccidioidomycosis infection in nonhuman primates, when properly controlled for, may not be a significant variable in HIV/AIDS pathogenesis or vaccine immunogenicity studies. Keywords: animal models; HIV/SIV disease pathogenesis; nonhuman primate models; vaccines; coccidioidomycosis; pigtail macaque; simian immunodeficiency virus; vaccine immunogenicity; HIV/AIDS; Valley Fever EN animal models HIV/SIV disease pathogenesis nonhuman primate models vaccines coccidioidomycosis pigtail macaque simian immunodeficiency virus vaccine immunogenicity HIV/AIDS Valley Fever 347 349 3 05/16/22 20220501 NES 220501 This letter expands on our previously published case report.[1] In this study, we determine if prior infection with coccidioidomycosis (Valley Fever) impacted study endpoints to investigate vaccine immunogenicity during simian immunodeficiency virus (SIV) infection as a model for immunizing people living with HIV/AIDS. [Extracted from the article]

Depletion of gut T helper 17 (Th17) cells during HIV infection leads to decreased mucosal integrity and increased disease progression. Conversely, T regulatory (Treg) cells may inhibit antiviral responses or immune activation. In HIV elite controllers, a balanced Th17/Treg ratio is maintained in the blood, suggesting a role for these responses in controlling inflammation and viral replication. HIV-infected individuals exhibit a range in responsiveness to combination antiretroviral therapy (cART). Given the link between the Th17/Treg ratio and HIV disease, we reasoned these responses may play a role in cART responsiveness. In this study, we investigated the relationship between the mucosal Th17/Treg ratio to acute simian immunodeficiency virus (SIV) viremia and the response to cART. Nineteen rhesus macaques were infected with highly pathogenic SIVΔB670 virus and cART was initiated 6 weeks postinfection. Mucosal CD4 T cell subsets were assessed by intracellular cytokine staining in the colon and mesenteric lymph nodes. Higher baseline Th17/Treg ratios corresponded with increased acute SIV viremia. Th17/Treg ratios decreased during acute SIV infection and were not restored during cART, and this corresponded to increased gut immune activation (Ki67+), markers of microbial translocation (sCD14), and T cell exhaustion (TIGIT+). Animals that maintained a more balanced mucosal Th17/Treg ratio at the time of cART initiation exhibited a better virological response to cART and maintained higher peripheral CD4 counts. These results suggest mucosal Th17 and Treg homeostasis influences acute viremia and the response to cART, a result that suggests therapeutic interventions that improve the Th17/Treg ratio before or during cART may improve treatment of HIV. [ABSTRACT FROM AUTHOR]

An abstract of the article "Rapid Loss of Th17 Cells after SIV Infection May Underlie Mucosal Dysfunction" by Laura E. Richert-Spuhler, Tiffany Hensley-Mcbain, Jillian Gile and colleagues is presented.